Mechanisms of Toll-Like Receptor 4 (TLR4)-Mediated Inflammation After Cold Ischemia/Reperfusion in the Heart | Zendy

David J. Kaczorowski | Zendy; Atsunori Nakao | Zendy; Raghuveer Vallabhaneni | Zendy; Kevin P. Mollen | Zendy; Ryujiro Sugimoto | Zendy; Junichi Kohmoto | Zendy; Brian S. Zuckerbraun | Zendy; Kenneth R. McCurry | Zendy; Timothy R. Billiar | Zendy

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Mechanisms of Toll-Like Receptor 4 (TLR4)-Mediated Inflammation After Cold Ischemia/Reperfusion in the Heart

Author(s) -

David J. Kaczorowski,

Atsunori Nakao,

Raghuveer Vallabhaneni,

Kevin P. Mollen,

Ryujiro Sugimoto,

Junichi Kohmoto,

Brian S. Zuckerbraun,

Kenneth R. McCurry,

Timothy R. Billiar

Publication year - 2009

Publication title -

transplantation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.45

H-Index - 204

eISSN - 1534-6080

pISSN - 0041-1337

DOI - 10.1097/tp.0b013e3181a36e5e

Subject(s) - ischemia , tlr4 , medicine , inflammation , cold ischemia , toll like receptor , receptor , reperfusion injury , cardiology , toll , immunology , innate immune system

Toll-Like Receptor 4 (TLR4) signaling mediates early inflammation after cold ischemia-reperfusion (I/R). We hypothesized that the TLR4 coreceptor CD14, the intracellular adaptor proteins myeloid differentiation factor 88 (MyD88) and TIR domain-containing-adaptor inducing IFNbeta (TRIF) would be required for cold I/R induced inflammation. High mobility group box 1 (HMGB1) is a putative endogenous activator of TLR4. Therefore, we also assessed the contribution of HMGB1 in cold I/R induced inflammation.

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